An interesting, manuscript accepted in the Journal of Infectious Diseases Oxford Academic by Lewnard and others published 9th March 2021 investigated the association.
They investigated Kaiser Permanente Healthcare members who were aged 65 or over as of 1st March 2020 and eligible for pneumococcal pneumonia vaccination.
Their study involved 531,033 individuals. They found that within this cohort receipt of the pneumococcal pneumonia vaccine PCV13 was associated with a lower incidence of any COVID-19 diagnosis, COVID-19 hospitalisation and fatal COVID-19.
Their results were consistent with previous findings of interactions between pneumococci and respiratory viruses contributing to the PCV efficacy against virus associated pneumonia amongst both children and older adults.
Their study supports the hypothesis that interactions with pneumococci in the upper airways contribute to SARS-CoV-2 pathogenesis in three respects:
- Similarity of the PCV13 effect estimates across all three outcomes suggesting that protection arose from the prevention at an early stage of COVID-19 pathogenesis rather than prevention of severe post-infection sequalae which would have led to a higher effectiveness against hospitalisation and death.
This finding is consistent with previous studies suggesting a low burden of secondary pneumococcal pneumonia following SARS-CoV-2 infection, in contrast to experience with other viral pathogens such as influenza.
- Receipt of PPSV23, which unlike PCV13 would not be expected to prevent pneumococcal colonisation, showed little association with protection against COVID-19 outcomes.
- Recent antibiotic prescription was a modifier of the PCV13 effects estimate. Individuals who had recently received antibiotics and who would therefore not be expected to carry pneumococci did not experience PCV13 associated protection against subsequent COVID-19 diagnosis.
The authors suggest that an improved understanding of viral bacterial interactions during SARS-CoV-2 infection remains necessary to validate the mechanistic basis for their findings.
However, their results are in agreement with other data suggesting that pathogenicity of respiratory viruses may be modified by bacterial carriage.
Evidence that upper respiratory commensal bacteria promote viral infection dates at least to 1987 with studies demonstrating that enzymes expressed by bacteria including pneumococci enhance influenza virus replication and pathogenicity.
More recently, the blunting of innate immune responses to influenza virus during pneumococcal colonisation has been demonstrated in human challenge studies.
Such mechanisms of interaction may account for epidemiological observations of enhanced virus acquisition and symptom risk amongst carriers of pneumococci and other respiratory commensal pathogenic bacteria.
The authors suggest that it is crucial to determine whether risk of SARS-CoV-2 infection and adverse clinical outcomes differ amongst those individuals who carry or do not carry pneumococci.
Pending further studies, The London General Practice encourages all appropriate vaccination schedules including pneumococcal pneumonia, influenza virus and SARS-CoV-2.
Dr Paul Ettlinger
BM, DRCOG, FRCGP, FRIPH, DOccMed